This document provides information about arterial blood gas analysis and interpretation. It includes: 1. Normal arterial blood gas value ranges for pH, PaCO2, PaO2, SaO2, HCO3, and other measures. 2. Guidelines on who may require an ABG, including patients on ventilators, with peritonitis or scheduled for surgery. 3. An overview of how to assess ABG results in terms of ventilation, oxygenation, and acid-base status. 4. Examples of ABG interpretations for different clinical scenarios.

1. Dr. T.R.Chandrashekar
Intensivist
Institute of Gastrointestinal diseases and Liver Transplant
(IGOT), Bangalore.
Arterial Blood Gas Analysis

2. pH 7.35 - 7.45
PaCO2 35 - 45 mm Hg
PaO2 70 - 100 mm Hg
SaO2 93 - 98%
HCO3
¯ 22 - 26 mEq/L
%MetHb < 2.0%
%COHb < 3.0%
Base excess -2.0 to 2.0 mEq/L
CaO2 16 - 22 ml O2/dl
Normal Arterial Blood Gas Values

3. Blood Gas Interpretation-means analyzing
the data to determine patient’s state of:
Ventilation
Oxygenation
Acid-Base

4. Who require ABG?
 1. 20 yr old OP poisoning pt on ventilator, SPo2
98% on 40% FIo2, ETCo2 40, hemodynamically
stable on PS/PEEP mode. ?
 2. 35 year old patients presents with peritonitis 2
days old,BP 110/60 mmHg, HR 130/mt, low
volume, RR 32/mt, SPo2 98% on 8/L oxygen on
RBM, ETCo2 40,Restless, Drowsy ?
 3. 50 yr old DM on insulin posted for LAP
cholecystectomy, Hb 10g/dL, BP120/80 mm/Hg,
HR 80/mt, Intra-operative bleeding about a litre
on GA ?

5. The Modified Allen Test ?
The modified Allen test. A, The hand is clenched into a tight fist and
pressure is applied to the radial and ulnar arteries. B, The hand is
opened (but not fully extended); the palm and fingers are blanched. C,
Removal of pressure on the ulnar artery should result in flushing of the
entire hand, within 15 to 20 seconds
Where do we do ABG?
There is insufficient evidence to support its systematic use before arterial puncture.
Radial artery
Femoral
Brachial
Dorsalis pedis

6. Approach to ABG Interpretation
Assessment
of Acid-Base
Status
Assessment of
Oxygenation &
ventilatory
Status
There is an interrelationship, but less
confusing if considered separately…..
Volume –
Osmolality
Electrolytes

7. … FIO2 = PaO2
-----XXXX Diagnostics----
Blood Gas Report
Measured 37.0 0C
pH 7.452
pCO2 45.1 mm Hg
pO2 112.3 mm Hg
Calculated Data
HCO3 act 31.2 mmol / L
O2 Sat 98.4 %
O2 ct 15.8
pO2 (A -a) 30.2 mm Hg 
pO2 (a/A) 0.78
Entered Data
FiO2 %
Ct Hb gm/dl
-----XXXX Diagnostics-----
Blood Gas Report
328 03:44 Feb 5 2006
Pt ID 3245 / 00
Measured 37.0 0C
pH 7.452
pCO2 45.1 mm Hg
pO2 112.3 mm Hg
Corrected 38.6 0C
pH 7.436
pCO2 47.6 mm Hg
pO2 122.4 mm Hg
Calculated Data
HCO3 act 31.2 mmol / L
HCO3 std 30.5 mmol / L
B E 6.6 mmol / L
O2 ct 15.8 mL / dl
O2 Sat 98.4 %
ct CO2 32.5 mmol / L
pO2 (A -a) 30.2 mm Hg 
pO2 (a/A) 0.78
Entered Data
Temp 38.6 0C
FiO2 30.0 %
ct Hb 10.5 gm/dl
pH………..7.40 (7.35-7.45)
PCO2 …..40 (35-45) mm of Hg
HCO3 …..24 (22-26) mEq/L
PO2 ……. 80-100 mm of Hg
O2 Sat…. >95
O2 Ct…. >18
Calculated parameters
Measured parameters
FIO2 X5=PaO2

8. Oxygenation

10. Matching delivery (DO2)
=
Requirement (VO2)
Function of Cardiorespiratory system
O2 delivery is a Cardio-Respiratory function
Microcirculation
BLOOD VOLUME

11. Hypoxemia
Shunt
Anemia
Reduced PaO2
Reduced CaO2
Micro circulatory
issues= VO2DO2= CaO2 X CO

12. O2
CO2
Alveoli
PAO2
Atmospheric air /FIO2
Water vapour is added-
Nose/ upper airway
Alveolar Oxygen
PaO2 (2% dissolved O2)
Measured in ABG
P(A-a)O2
SaO2
O.
D.
C.
Temp
H+
2,3-DPG
98% of O2 is Hb bound-
1.34 x Hb% x Sao2CaO2-oxygen content +PaO2 x 0.003ml=
PAO2 ?
PaO2 ?
SaO2 ?
CaO2 ?
Which should be used?
98% of O2 is Hb bound
DaO2-Oxygen delivery- CaO2 x Cardiac output
(2% dissolved O2)
DO2=VO2

13. O2
PaCO2=60 mmHg
PAO2 = FIO2 (BP-47) – 1.2 (PaCO2)
=.21 (760-47) – 1.2 (60)
= 150 – 72 = 78
An elevated PaCO2 will lower the PAO2
and as a result will lower the PaO2
FIO2
We always correlate PaO2 with
FiO2
BUT………………………….
never forget to correlate with
PaCO2
PAO2=FIO2(Barometric Pressure-H2O)-1.2(PCO2)
PAO2 = FIO2 (760– 47 mm Hg)- 1.2 (PaCO2)
PAO2 = 0.21(713)-1.2(40)=100 mmHg
“1.2” is dropped when FIO2 is above 60%.
5 X FIO2=PaO2
1 mm rise of PaCO
2
decreases PaO
2
by 0.9 in alveolar sac

14. A-aDo2
A-aDo2 = PAO2-PaO2(from ABG)= 10-15 mmHg / Increases with age
Increased P(A-a)O2 -lungs are not transferring oxygen properly from
alveoli into the pulmonary capillaries.
O2
CO2
PaO2
Alveoli
PAO2
P(A-a)O2
Diffusion defect
V/Q Mismatch-Dead Space
Shunt
P(A-a)O2 signifies some sort of
problem within the lungs
A normal A-a gradient
Responds to O2

15. Alveolar-arterial Difference (10mm Hg)
O2
CO2
Alveolar – arterial G.
100 - 45 = 55
……………….Wide A-a
Oxygenation
Failure
Wide Gap
PCO2 = 40
PaO2 = 45
PAO2 = 150 – 1.2 (40)
= 150 - 50
= 100
Ventilation
Failure
Normal Gap
PCO2 = 80
PaO2 = 45
PAO2 = 150-
1.2(80)
= 150-100
= 50
Alveolar arterial G.
50 – 45 = 5
…………….Normal A-a

16. Oxygen Dissociation Curve: SaO2 vs. PaO2
CaO2
A B
5 g/dl 2.5g/dl
65 ml/L 35 ml/L

17. DO2=VO2
 Lactate
 ScVO2/SVO2
 A central venous ABG may be more informative
than arterial ABG????

18. 65 yr old male with DM IHD –in septic
shock on ventilator
ABG-PaO2-90 PH 7.42, PCO2 43
Hb-12 gm%, Spo2 98%
CaCo2-17 Vol%
BP 90/40 mmHg ,Temp 103F
What is the problem ?
ScVO2 48%, Lactate 8 mMoles/L
Fluids
Nor adrenaline / Dobutamine
Fever control
After 2hrs
ScVO2 68%, Lactate 2 mMoles/L
Case ….
65 yr old male with DM IHD –in septic
shock on ventilator
ABG-PaO2-90 PH 7.42, PCO2 43
Hb-12 gm%, Spo2 98%
CaCo2-17 Vol%
BP 70/40 mmHg ,Temp 102F
What is the problem ?
ScVO2 35% Lactate 10 mMoles/L
Microcirculatory Mitochondrial
Dysfunction (MMDS)
Prognostic indicator-LACTI- TIME

19. ? (A-a)O2 difference
FIO2 = 1.0
Increased Normal
Hypoventilation
responsive response
Low V/Q Shunt
Hypoxemia

20. Assessment of Oxygenation
 Alveolar oxygen( PAO2 )is a calculated parameter
 True or False
 Write the PAO2 equation
 PAO2=FIO2(Barometric Pressure-H2O)-1.2(PCO2)
 “1.2” is dropped when FIO2 is above 60%.

21. Oxygenation problems
 FIO2 = 1.00, PaCO2 = 30 mm Hg
 PAO2 = 1.00 (713) - 30 = 683 mm Hg
 PaO2 is 100
 A-a difference= 683-100= 583
 ARDS patient on ventilator
 SHUNT

22. Problems: Oxygenation
 Room Air, PaO2 = 45, PaCO2 = 45
 PAO2 = 150 - 1.2(45) = 96
 P(A-a)O2 = 96 - 45 = 51
 Now on 100% O2, PaO2 =555, PaCO2 = 48
 PAO2 = 1.0(760 - 47) - 1.2(48) = 655
 P(A-a)O2 = 655 - 555 = 100
 Dramatic increase in PaO2
 V/Q mismatch major cause of hypoxemia

23. FIO2 = .21, PaCO2 = 50 mm Hg
 PAO2 = .21 (713) - 1.2 (50) = 90 mm Hg
 PaO2 is 80
 Calculate A-a difference-90-80=10
 what is your inference?
FIO2 = .40, PaCO2 = 30 mm Hg
 PAO2 = .40 (713) - 1.2 (30) = 249 mm Hg
 PAO2 > PaO2 True or False

24. PaO2/FIO2 ratio
 Calculate PaO2/FIO2 ratio
 FIO2= 40%, PaO2 200= 500
 200/0.4= 500
 FIO2= 100%, PaO2 60= 60= 60/1
 Define ARDS on PaO2/FIO2 ratio
PaO2/FIO2
200- 300
PEEP≥ 5 cm H2O
PaO2/FIO2
100- 200
PEEP≥ 5 cm H2O
PaO2/FIO2
≤100
PEEP≥ 10 cm H2O
Mild Moderate Severe

25. Calculate oxygen content.
 Write down Oxygen content formula
 CaO2 = quantity O2 bound + quantity O2
dissolved
to hemoglobin in plasma
CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2)
 In ABG PaO2 is a measure of what ?
 Is SaO2 measures or calculated in ABG?
 DO2 formula= CaO2 X CO

26. Which patient is more hypoxemic, and why?
 Patient A: pH 7.48, PaCO2 34 mm Hg, PaO2 85 mm Hg, SaO2
95%, Hemoglobin 7 gm%-
 Patient B: pH 7.32, PaCO2 74 mm Hg, PaO2 59 mm Hg, SaO2
85%, Hemoglobin 15 gm%-
 Patient A:
Arterial oxygen content = .95 x 7 x 1.34 = 8.9 ml O2/dl
 Patient B:
Arterial oxygen content = .85 x 15 x 1.34 = 17.1 ml O2/dl
Hypoxic/Hypercarbic
Anemic
98% of O2 is Hb bound-
1.34 x Hb% x Sao2
+ ( 2% )PaO2 x 0.003mlCaO2 =

27. Matching DO2 to VO2
 Which are the two parameters used to identify
this?
 Septic patient admitted to ICU, looks dry,
capillary refill time increased, dark colured urine,
restless, BP 80/50, HR 150/mt
 ScVO2-45%, Lactate 6 mmol/L, PH 7.16,
PaO2/PCO2- 68/39 mmHg, HCO3 12
 What are the clinical signs hypoperfusion?
 Can they used to assess hypoperfusion?
 Fluids?--Which/ how much?

28. After 2hrs
If BP does not increase
after 2L of fluids
What next?
a) After 2hrs- fluid
resuscitation/Noradrenaline
, BP140/80 mmHg,ScVo2-
65%, Lactate 3 mmol/L
What is your inference?
After 2hrs- fluid
resuscitation/Noradren
aline, BP 70/40
mmHg, ScVo2-45%
Lactate 9mmol/L
MMDS

29.  Can a patient have high lactate and show
improvement?
 Can a patient have normal lactate and
deteriorate?
 Is Lactate normalization time a good prognostic
indicator?
 What is the acid base diagnosis?


30. Capillary
Arteriole
Neutrophil
Aggregation
Vasoconstriction
Endothelial Cell
Destruction
Venule
Cell
Due to interstitial
edema increased
distance impairing
oxygenation
Micro emboli
O2
lactate
CO2
v
Microcirculatory abnormalities If not recognized early and
corrected leads to organ
injury and ultimately death
1.Normal lactate/ patient sick?
2. High lactate/ Patient improving?
MMDS

31. Assessment of Ventilatory Status….

32. Oxygenation Acid-Base
HCO3
PAO2 = FIO2 (BP-47) – 1.2 (PCO2) pH ~ ------------
PaCO2
PaO2
» VCO2 x .863
» PaCO2 = --------------------
» VA
» VA=Minute ventilation-Dead space volume
» f(VT) – f(VD)
PaCO2 is key to the blood gas universe; without understanding
PaCO2 you can’t understand oxygenation or acid-base.
 The ONLY clinical parameter in PaCO2 equation is RR
VCO2=CO2 production

33. VCO2 x 0.863
PaCO2 = ------------------
VA
 Alveolar ventilation= Minute ventilation – Dead space volume
 VCO2 increased production in catabolic states, fever, pain etc
PaCO2 = Inversely proportional to alveolar ventilation
Not on Minute ventilation which is measured
Dead space quantification at bed side not possible
VCO2 cannot be estimated at bedside
Hypercapnia (cont)
Sedation , central causes, ARDS
ventilation, muscle paralysis COPD

34. Clinical Assessment of Hypercapnia is Unreliable
There is no predictable correlation between PaCO2 and the
clinical picture.
In a patient with possible respiratory disease, respiratory rate,
depth, and effort cannot be reliably used to predict even a
directional change in PaCO2.
A patient in respiratory distress can have a high, normal, or
low PaCO2. A patient without respiratory distress can have a
high, normal, or low PaCO2.

35. Condition State of
PaCO2 in blood alveolar ventilation
> 45 mm Hg Hypercapnia Hypoventilation
35 - 45 mm Hg Eucapnia Normal ventilation
< 35 mm Hg Hypocapnia Hyperventilation
PaCO2 abnormalities…
PCO2-65 mmHg with rate 7/mt in Drug overdosage
65/7-true hypoventilation
PCO2-65 mmHg with rate 37/mt in COPD pt
65/37- Reduced alveolar ventilation/ dead space ventilation
PCO2-35 mmHg with rate of 37/mt in post operative patient
with pain and fever-Increased CO2 production

36. Po2 is 60,
PCo2 is 68
Increase Vt
to 500ml
Increase
RR 15
After one hr repeat ABG shows PO2 of 58
PCO2 of 83
COPD on ventilator on VC
Vt 400ml, Fio2 40%, PEEP 4 cms H2o
RR10/mt, I:E 1:2 Minute ventilation
of 500x10=4000
Minute ventilation of
500x15=7500

37. Why this happened?
 If 400ml is not able to come out in 4 seconds
 How 500ml will come out in 2.6seconds
 60/15=4seconds I:E ratio 1:2=1.3:2.6 seconds
Leads to more Air trapping
Air trapping
Alveoli
compress the
capillary
Dead Space

38. 400ml
500ml
4 seconds 2.6 seconds
May be 350ml may
decrease your PCO2
Minute ventilation is the main determinant
of air trapping

39. Why does this air trapping
increase CO2 (Dead space)?
 Alveoli become distended hence less
space to fresh air & decreased
compliance
 Distended Alveoli compresses alveolar
vessels
 Increased PVR
 Decreased compliance and compressed
vessels V/Q mismatch
 Increased Dead space

40. CO2 removal is inversely proportional
to Minute Ventilation
CO2 removal is inversely proportional to
Effective Alveolar Ventilation
Effective Alveolar Ventilation
=
Minute Ventilation – Dead Space Ventilation

41. Effective Alveolar ventilation
 Vt=400ml
 RR=10
 MV=4l
 EAV=MV-Dead space
 Dead space ventilation
=150x10=1.5l
EAV=4l-1.5l=2.5l
 Vt-500ml
 RR= 15
 MV=7.5l
 EAV=MV-Dead space
 Dead space ventilation
=400x15=6l
EAV=7.5l-6l=1.5l
In controlled ventilation-Decrease tidal volume, increase E time,
In PS mode- Increase peak flow and increase expiratory sensitivity to 40%

42. Minute ventilation
Tidal volume=6-7ml/kg
Rate 16/mt, IC is reduced
Low minute ventilation leads to ↑PCO2 which is the
price we pay for preventing DH,
In fact current literature suggests that risk
of dynamic hyperinflation is much larger
than those of permissive hypercapnia.
Target Normal PH not CO2
ABG –PH-7.31,
PCO2-65mmHg,
Pao2-69mmHg,
HCO3 32

43. Shibu lijack
Acid Base analysis

44. Basics
•[H+]= 40 nEq/L at pH-7.4
•For every 0.3 pH change = [H+] double
160nEq/L
40 nEq/L
16nEq/L
[ H+] in nEq/L = 10
(9-pH)

45. Acid-Base Physiology

46. CO2 + H2O H2CO3 H+ + HCO3
-
CO2
H+
HCO3
-
Acid-Base physiology
Respiratory
Metabolic
Ventilation controls PCO2
Kidney losses H+ and reabsorbs bicarbonate (HCO3-)
Bicarbonate is the transport from of CO2 hence should move
in the same direction
PCO2-Respiratory acidosis
(Hypoventilation)
PCO2-Respiratory alkalosis
(Hyperventilation)
HCO3- Metabolic acidosis
HCO3- Metabolic Alkalosis
Starts within
minutes good
response by
2hrs,
complete by
12-24 hrs
Starts after few
hrs complete
by 5-7 days
Phosphate and Protein buffer

47. Acid-base Balance
Henderson-Hasselbalch Equation
[HCO3
-]
pH = pK + log -------------
.03 [PaCO2]
For teaching purposes, the H-H equation can be
shortened to its basic relationships:
HCO3
- ( KIDNEY)
pH ~ --------------------
PaCO2 (LUNG)
Maximum compensation
HCO3-= 40/10
CO2=60/10

48. Characteristics of  acid-base disorders
DISORDER PRIMARY
RESPONSES
COMPENSATORY
RESPONSE
Metabolic
acidosis
 PH  HCO3
-  pCO2
Metabolic
alkalosis
 PH  HCO3
-  pCO2
Respiratory
acidosis
 PH  pCO2  HCO3
-
Respiratory
alkalosis
 PH  pCO2  HCO3
-

49. Respiratory
Respiratory Acid is CO2
Increased CO2-Acidosis Decreased CO2- Alkalosis
Acute and Chronic
1. Acute Respiratory Acidosis
2. Chronic Respiratory Acidosis
3. Acute Respiratory Alkalosis
4. Chronic Respiratory Alkalosis
Hypoventilation Hyperventilation
H+
HCO3
-
Metabolic
Compensation

50. Compensation for changes in CO2
RESPIRATORY disorders…
Expected HCO3 for a Change in CO2 ......... 1 2 3 4
what has changed ? CO2

51. Metabolic change
H+
HCO3
-
Metabolic
HCO3- Metabolic acidosis
HCO3- Metabolic Alkalosis
Hypoventilation to increase CO2 to reduce pH
Metabolic Alkalosis –pH high, HCO3 high
Metabolic acidosis –pH low, HCO3low
Hyperventilation to decrease CO2 to increase pH
CO2

52. Winters’ formula
pCO2 = 1.5 x [HCO3-] + 8 ± 2
Last two digits of pH = PaCO2
pH being 7.23 = PaCO2should fall to 23mmHg
Metabolic Alkalosis
PCO2 = 0.7x [HCO3-] + 20 ± 5
For every 10 increase in HCO3 = PCO2 increases by 6
Unpredictable because increasing CO2 causes RR
Last two digits of pH = PaCO2
pH being 7.56 = PaCO2should fall to 56 mmHg
Metabolic Acidosis

53. Body’s physiologic response to Primary disorder
in order to bring pH towards NORMAL limit
Full compensation
Partial compensation
No compensation…. (uncompensated)
BUT never overshoots,
If a overshoot pH is there,
Take it granted it is a MIXED disorder
Normal functioning

54. Metabolic alkalosis
Primary accumulation of serum bicarbonate (HCO3
-)
Low urinary Chloride
< 20meq/L
High urinary Chloride
> 20meq/L
The most common causes are volume
depletion (particularly when involving loss
of gastric acid and chloride (Cl) due to
recurrent vomiting or nasogastric suction)
and diuretic use.
Intracellular shift of H+
Hypokalemia / Hypomagnesemia
Renal H+ loss
Primary mineralocorticoid excess
Fluid correction with Normal saline
Hypokalemia- KCL
Dilute 0.1 N HCL/oral NH4CL
Correction of hyperaldosteronism

55. If a overshoot pH is there,
Take it for granted it is a MIXED disorder
Simplified rules predict the pH and HCO3
- for a given change
in PaCO2. If the pH or HCO3
- is higher or lower than expected
for the change in PaCO2, the patient probably has a metabolic
acid-base disorder as well.
In maximally-compensated metabolic acidosis, the numerical
value of PaCO2 should be the same (or close to) the last two
digits of arterial pH
Clues for mixed disorders…

56. H+
HCO3
-
Metabolic
Loss of HCO3
- may result from
Renal loss in Proximal renal tubular acidosis.
Gastrointestinal loss in diarrhea
Over production Ketoacids or lactic acid
Decreased renal excretion of hydrogen ion as in
uremic acidosis and distal (type I) renal tubular
acidosis.
Metabolism of ingested toxins such as methanol,
ethylene glycol, and paraldehyde
Primary reduction in serum bicarbonate (HCO3
-)
Metabolic acidosis-Definition

57. Metabolic acidosis-
compensatory response
DISORDER PRIMARY
RESPONSES
COMPENSATORY RESPONSE
Metabolic
acidosis
 PH  HCO3
-
The PaCO2 begins to fall within 1–2hr
Should reach a steady–state value by 12–24hr
If not patient has hypoventilation- Resp Acidosis
 pCO2

58. Diagnosis of metabolic acidosis
 History
 40 year old patient presents with 3 day old
peritonitis septic BP 80/60mmHg
 RR 40/min
 Metabolic acidosis
• ABG- pH 7.21 / PCO2 = 22 / HCO3- = 9 mEq/l
• Lactate 6 mmol/L
• Post operative cardiac arrest
• Metabolic + Respiratory acidosis

59. Metabolic acidosis-is suspected when
 HCO-
3 is low
 Serum chloride is elevated
 Always calculate Anion gap
 Increased Anion gap
 There is electrochemical balance
 Sum of all negatively charged electrolytes (anions) =
Sum of all positively charged electrolytes (cations).
 More anions are unmeasured than are cations
 Anion gap is thus an artifact of measurement, and not
a physiologic reality
???

60. More anions are unmeasured than are cations
 Major unmeasured anions
• albumin
• phosphates
• sulfates
• organic anions- ketones and
lactate
Anion gap …
1 gm/dl decrease in serum albumin causes
a 2.5 mEq/L drop in the AG

61. Anion gap is based on only three
electrolytes:
sodium, chloride and bicarbonate
 AG = [Na+] - [Cl- +HCO3
-] =
 140 - 128 = 12mEq/L
(venous CO2 = HCO-
3 can be use

62. Pathogenesis of Metabolic Acidosis
with AG
Fixed acid accumulation and low serum bicarbonate
Renal failure Renal,GI Lactic Salicylate
Ketones Methanol
Phosphate Ethylene glycol
HCl
AG = [Na+
] - [Cl-
+HCO3-
]

63. Method to identify mixed disorders in
elevated Anion gap Metabolic acidosis
The Delta GAP
The net effect will be an increase in unmeasured anions
by the one acid anion A- (ie anion gap increases by one)
and a decrease in the bicarbonate by one meq.
If Anion gap-12= x
HCO3 should be 24-x
If Anion gap-12= x
HCO3+X= 24
<24 Non gap Acidosis
>24 Metabolic alkalosis+ EGMA

64. Delta GAP
 Normal Anion gap is 12 to 14
 As we have already understood- this AG is
accounted by unmeasured ion. If there is a real
AG, it will be >12
 For every H+ ion produced= to neutralise this
HCO3 is consumed.
 So rise in H+= fall in HCO3-
 Any value of AG more than 12= equal decrease in
HCO3 from its normal value of 24
 Or to make things simple
 Increased AG value = measured AG-12
 When added up to HCO3 values=24

65. Delta gap
 AG-12 + HCO3= 24
 <24 =more + ions are present=Hence acidosis=
Non gap Acidosis
 >24 more – ions are present=
alkalosis=Metabolic alkalosis
 And there is already increased AG, we have
Elevated gap Metabolic acidosis

66. 32 yr old pregnant patient admitted to ICU with
4 days non stop vomiting HR 145/mt, BP 78/42
Case
pH 7.41 Normal
PCO2 42
HCO3 26
Sodium 146
Chloride 92
Elevated Gap metabolic acidosisAnion Gap 146-(92+26)=28
Delta gap 28-12=16+ HCO3=16+26=42 Metabolic alkalosis
Normal
Normal

67.  Excessive normal saline infusion
 Chronic kidney disease
 Adrenal insufficiency (primary or
secondary)
 Diarrhea
 Intestinal, pancreatic, or biliary
fistulae
 Proximal RTA // Distal RTA
 Ureterosigmoidostomy /
Ureteroileostomy
 Methanol intoxication
 Uremic acidosis
 Diabetic ketoacidosis
 Paraldehyde intoxication
 Iron/ INH
 Lactic acidosis
 Ethylene glycol
intoxication
 Salicylate intoxication
Causes of metabolic acidosis
Increased anion gap
Normal (hyperchloremic) anion
gap

68. ABG interpretation
Patient history most important
ABG with FIO2
Serum electrolytes
Urine electrolytes
Serum and urine osmolality

70. 2. Look at pH?
3. Look up HcO3-// PCo2
4. Match either CO2 or the HCO3 with pH
5. Fix the level of compensation.
6.If metabolic acidosis, calculate-Anion Gap
7.If Anion gap present calculate Delta Gap
1. Consider the clinical settings! Anticipate the disorder
7 steps to analyze ABG

71. Importance of history in reading ABG
 Patient had a cardiac arrest, CPR done, patient
resuscitated successfully,
 What abnormalities do you expect?
 Metabolic Acidosis and respiratory Acidosis
 Write down a ABG which correlates to that
history
 pH----------- 6.89
pCO2 -------70
pO2 ---------42
HCO3------- 13

72. First Step-Clinical History
 COPD- Chronic
 Respiratory Acidosis-Met alkalosis
 Asthma-Acute
 Respiratory Acidosis not well compensated
 Diabetes- Ketoacidosis
 Cardiac arrest-Acute
 Metabolic/Respiratory acidosis
 Septic shock-/ AKI
 Metabolic acidosis
 CNS- Metabolic alkalosis

73.  50 yr old DM poorly controlled, dehydrated BP
90/60 mm/Hg
 ABGpH 7.26
PCO2 25
HCO3 8
Sodium 136
Chloride 101
1. Label pH
What is the pathology you are anticipating? Metabolic acidosis

74. 7.55
7.54
7.53
7.52
7.51
7.5
7.49
7.48
7.47
7.46
7.34
7.33
7.32
7.31
7.30
7.29
7.28
7.27
7.26
7.25
7.24
The second step
Look at the pH - Label it.
7.45
7.44
7.43
7.42
7.41
7.40
7.39
7.38
7.37
7.36
7.35
pH
pH 7.26 Acidotic
PCO2 25
HCO3 8
Sodium 136
Chloride 101

75. 2-Look at -pCO2. Label it
3-look at the HCO3- Label it.
The third and fourth step
pH 7.26 Acidotic
PCO2 25 Alkaline
HCO3 8 Acidotic
Sodium 136
Chloride 101
Which is moving in the direction of the pH
Is the primary disorder

76. Body’s physiologic response to Primary disorder
in order to bring pH towards NORMAL limit
Full compensation
Partial compensation
No compensation…. (uncompensated)
Never corrects to normal pH,
If a overshoot pH is there,
Take it granted it is a MIXED disorder
Normal functioning

77.  Metabolic Acidosis & metabolic Alkalosis
 For full correction
 Last two digits of pH= PCO2
Metabolic pathology PCO2 correction
pH 7.26 Acidotic
PCO2 25 Alkaline
HCO3 8 Acidotic
Sodium 136
Chloride 101
7.26=25
STEP-4

78. Calculate compensation
 Chronic COPD with
pH 7.32 Acidosis
PCO2 68 RES Acidosis
HCO3 32 Comp Alkalosis
68-40=28
2.8 x 3=8.4
24+8.4=32.4

79. 5th step- GAP
pH 7.26 Acidotic
PCO2 25 Alkaline
HCO3 8 Acidotic
Sodium 136
Chloride 101
Anion Gap= Na- (Cl+ HCO3)
136-(101+8)=27
Elevated Anion gap metabolic acidosis
Delta gap
27-12=13
HCO3 should be 24-13=11
HCO3 + AP= 24
13+8=21
Non Anion gap metabolic acidosis

80. pH 7.50 Alkalotic
PCO2 20 Alkalotic
HCO3 18 Alkalotic
Sodium 143
Chloride 100
40 yr old male pt admitted to ICU three hr
back was normal, history of altered mental
status vertigo and vomiting, RR 35/mt
Anion Gap= Na- (CL+ HCO3)
143-(100+15)=23
Elevated Anion gap metabolic acidosis
Delta gap
23-12=11
HCO3 should be
24-11=13
HCO3 + AP= 24
11+18=29
Metabolic
alkalosis

81. Finally

82. Importance of history in reading ABG
 Patient had a cardiac arrest, CPR done, patient
resuscitated successfully,
 What abnormalities do you expect?
 Metabolic Acidosis and respiratory Acidosis
 Write down a ABG which correlates to that
history
 pH----------- 6.89
pCO2 -------70
pO2 ---------42
HCO3------- 13

83. Write a clinical scenario ?
Normal pH
Ac
If the patient has a chronic COPD
HCO3 should change 3 for every 10 increase in PCO2
67-40=27
2.7 x 3=8
HCO3=24+8=32 but is 42 so pt has metabolic alkalosis
Add vomiting
Then the clinical picture adds up
Anion gap140-(88+47)=5

84. A 45-year-old man is admitted to the hospital with severe diarrhea
Metabolic acidosis
Well compensated
Normal anion gap
Case-1
pH 7.26 Acidotic
PCO2 25
HCO3 11
Sodium 133
Chloride 110
Anion GAP= 133-(110+11)=12

85. A 35-year-old woman is brought to the emergency room in a
comatose state. According to her sister, she had been complaining of
progressive weakness for 2 months. On examination, the patient was
responsive only to painful stimuli, blood pressure was 70/40 and
respiratory rate was 10 and shallow; she had no peripheral edema.
The deep tendon reflexes were absent; muscle strength was not
testable
This is a mixed metabolic and respiratory acidosis
pH 6.88 Acidotic
PCO2 40 Normal
HCO3 7 Acidotic
Sodium 135
Chloride
K
118
1.5
PCO2= 10 is 40 so has respiratory acidosis
Anion gap =135-(118+7)=10
Case-2

86. Normal A.B.G.
pH = 7.4
PaCO2 = 40
HCO3 = 24
Case-3

87. compensated Metabolic
Acidosis
pH = 7.4
PaCO2 = 40
HCO3 = 24
20 yr old male with Acute Gastroenteritis…..
Case-4

88. A 46-year-old man has been in the hospital two days with
pneumonia. He was recovering but has just become
diaphoretic, dyspneic, and hypotensive. He is
breathing oxygen through a nasal cannula at 3 l/min,
RR 30/mt.
Case-5
Combined respiratory
alkalosis and
metabolic acidosis.
Hyperventilating on
40% O2=80mm Hg
pH 7.40 Normal
PCO2 20 Alkaline
HCO3 12 Acidotic
PaO2 80 Hypoxic
Hb 13.3g% CaO2 17.2 ml O2/dl

89. A 23-year-old man is being evaluated in the emergency room for
severe pneumonia. His respiratory rate is 38/min and he is
using accessory breathing muscles.
Case-6
Delta gap
37-23=14
14+23=37
Patient has respiratory acidosis, metabolic acidosis, and metabolic alkalosis.
FIO2 90%
pH 7.41 Normal
PaO2 47 PaO2/FIO2 ?
PCO2 55 RR 38
SaO2 86%
HCO3 23
CaCO2 15.8 ml O2/dl ok
Sodium 132
Chloride 72
AG 132-(72+23)=37

90. Case-7
 A 50 year old insulin dependent diabetic woman
was brought to the ED by ambulance. She was
semi-comatose and had been ill for several days.
Current medication was digoxin and a thiazide
diuretic for CHF.
History:
Elevated anion gap
acidosis secondary to
DKA
Metabolic alkalosis in
the setting of thiazide
diuretics use.
Urine ketones 3+ Suspect ??
pH 7.29
PaO2 82
PCO2 32
HCO3 19
Glucose 615
Sodium 154
Chloride 100
AG Delta Gap 35-12=23 + 19=42 Met alk
Mixed elevated anion gap metabolic acidosis and metabolic
alkalosis likely due to DKA and thiazide diuretics
154 -(100 + 19) = 35

91. A 61 year old obese COPD patient with
CHF was shifted to ICU
Normal
Resp acidosis
Metabolic alkalosis
Anion Gap132-(92+34)=6
Respiratory Acidosis+ metabolic alkalosis
Case-8

92. 32 yr old pregnant patient admitted to ICU with
4 days non stop vomiting HR 145/mt, BP 78/42
Case-9
pH 7.41 Normal
PCO2 42 Normal
HCO3 26 Normal
Sodium 146
Chloride 92
Anion Gap 146-(92+26)=28
Elevated Gap metabolic acidosis
Delta gap 28-12=16+ HCO3
16+26=42
Metabolic alkalosis

93. 40 yr old male pt admitted to ICU was apparently alright
three hr back, with history of altered mental status vertigo
and vomiting
pH 7.50 Alkalotic
PCO2 20 Alkalotic
HCO3 15 Acidosis
Sodium 143
Chloride 100
Anion gap143-115=28
Elevated gap metabolic Acidosis
Delta gap=28-12=16
16+15=31 metabolic alkalosis
Elevated gap metabolic Acidosis
Metabolic alkalosis
Resp alkalosis
PCO2 40-
20=20 =
2x 3=6
HCO3 =
24+6= 30

94. Case-10
50 yr old DM on insulin posted for LAP cholecystectomy, Hb
10g/dL, BP120/80 mm/Hg, HR 80/mt, Intra-operative bleeding
about a 2litre, On GA
BP 60/40 mm/Hg
HR=130 /mt
Hb= 6.5g/dL
Calculate oxygen content
ECG shows mild ST elevation
Acidosis
Metabolic
GA
Anion Gap=140-(92+18)= 30
Delta gap
30-12=18
24-18=6
18+18=36
EGMA+M Alkalosis
Fluids or blood
FFP/platelets/Cryo?
Fluids NS or RL?
Can we decrease PCO2?
NAHCO3?
Vasopressor?
Inotrope or esmolol?

95. Case -11
A patient presents with:
pH 7.15 Acidotic
PCO2 18 Alkalotic
HCO3 6 Acidotic
Sodium 135
Chloride
AG
14
135 - (6 + 114) = 15

97. Problems: Oxygenation
 Room Air, PaO2 = 45, PaCO2 =30
 PAO2 = 150 – 1.2(30) = 114 mm Hg
 P(A-a)O2 = 114 - 45 = 69 elevated
 Now on 100% O2, PaO2 = 65, PaCO2= 32
 PAO2 = 1.0(760 - 47) - (48) = 665
 P(A-a)O2 = 665 - 65 = 600
 minimal elevation in PaO2
 shunt major cause of hypoxemia
ARDS pt on ventilator on 100%
FIO2 and Vt 6ml/kg